About Left Ventricular Torsion,

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EDITORIAL

About left ventricular torsion, sex differences,

shear strain, and diastolic heart failureThierry C. Gillebert * and Nico R. Van de VeireHeart Center, Faculty of Medicine and Health Sciences, University of Ghent, De Pintelaan, 185, 9000 Ghent, Belgium

This editorial refers to Preserved left ventricular twistand circumferential deformation, but depressed longitudi-nal and radial deformation in patients with diastolic heartfailure by J. Wang et al. , on page 1283

An attempt at visualizing the Fourth Dimension: Take a point, stretchinto a line, curl it into a circle, twist it into a sphere, and punch through the sphere. Albert Einstein

Wang et al.1 provide novel pathophysiological information onpatients with diastolic heart failure, by exploring the fourth dimen-sion of cardiac function: left ventricular (LV) twist. The complexactive and passive physiological events occurring during the heartcycle are related to the complex structure of the heart, which isa helix that contains an apex. Lower (17th century) described the cardiac helix form as having an apical vortex, in which the

muscle bres go from outside in, in a clockwise way, and frominside out, in a counter-clockwise direction. 2 Nature containsmany pathways of clockwise and counter-clockwise spirals (reci-procal spirals), e.g. the ower buds of a daisy, the sea shell, andeven human ngertips. Dr Torrent-Guasp compared the structureof the heart with a coiled rope with a beginning and an end at theaorta and pulmonary artery; a wraparound loop called a basal loop;and a helix that he called the apical loop. 3 Does this ventricular architecture correspond to a functional reality? The classical viewrelates to contracting and relaxing, as dened by William Harvey(1628): constricting to narrow and eject, dilating to widen andll. In a comprehensive review, Dr Buckberg describes that theheart cycle is not merely constricting and dilating but that it com-prises four fundamental motions that include narrowing, shorten-ing, lengthening, and widening.2 The initial contraction involves the basal loop that causes constriction whereby a stiff outer shellmuscle is formed that surrounds both ventricles. This corresponds to the isovolumetric, pre-ejection phase of systole. The nextsequence is the contraction of the descending loop, which twistsdownward to thicken and cause ejection. Contraction of theascending segments starts shortly after the descending segment

and persists after the descending segment contraction stops, 4 pro-ducing untwisting (isovolumetric relaxation) and creating suction(early lling). Finally, relaxation is completed, and passive llingof the ventricles and atrial contraction occur. As viewed from the LV apex, the early-systolic shortening of subepicardial bresresults in a counter-clockwise rotation of the LV apex and a clock-wise rotation of the LV base. The net result is a twist that results ina wringing movement of the LV. 5 During isovolumetric relaxation, the twisted subendocardial bres behave like a compressed coil that springs open while releasing the potential energy stored in the deformed matrix. This recoil is appreciated from the apex asa clockwise rotation of the LV apex.In the case of heart failure with diminished ejection fraction, thehelical formation of the heart is replaced by a spherical chamber causing a diminished capacity to shorten and lengthen. Whenheart muscle bres adopt a spiral formation, proceeding toward

the apex, 15% bre shortening causes a 60% LV ejection fraction.If bre orientation is horizontal or transverse, the same 15% breshortening produces only a 30% ejection fraction. 6 The underlyinganatomy of heart failure with diminished LV ejection fraction mayreect changing the oblique apical loop into a more transversebasal loop architecture, with resultant diminished function.

Until now, the lack of easily applicable non-invasive techniques to study the LV myobre architecture in relation to the spatiotem-poral sequence of regional deformations occurring during cardiaccontraction and relaxation has prohibited extensive in vivoexper-iments, especially in patients with diastolic heart failure. A recentlyintroduced echocardiographic techniquespeckle tracking enables non-invasive evaluation of these complex cardiac events.Speckle tracking or two-dimensional strain is a technique that tracks frame-to-frame movement of natural acoustic markers, or speckles, present on standard two-dimensional ultrasound tissueimages.7 Local two-dimensional tissue velocity vectors arederived from the spatial and temporal data of each speckle. Myo-cardial strain can be assessed from temporal differences in themutual distance of neighbouring speckles. From short axisimages, circumferential and radial strain can be calculated and,

The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.

* Corresponding author. Tel: 32 9 240 3481, Fax: 32 9 240 4432, Email: [email protected] doi:10.1093/eurheartj/ehn141

Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2008. For permissions please email: [email protected].

European Heart Journaldoi:10.1093/eurheartj/ehn173

European Heart Journal Advance Access published April 23, 2008
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from apical images, longitudinal strain can be derived. This allowsnon-invasive evaluation of longitudinal shortening, radial thickening,and circumferential shortening of myocardial muscle. Moreover,speckle tracking was also validated for the measurement of cardiac rotation and twist. 8 It is simple and reproducible: it onlyrequires two-dimensional acquisition of parasternal short axisimages at the basal level and the apical level. Apical and basal

rotation is measured from frame-to-frame tracking of grey-scalespeckle patterns. LV twist is calculated as the difference in rotationbetween the apex and the basal segment. LV torsion and twist arenot interchangeable, as torsion represents twist normalized for distance.

In their study, Wang et al.1 showed that in patients with systolicheart failure, longitudinal, circumferential, and radial strain, and LV twist all are impaired. In contrast, in patients with diastolic heartfailure, LV longitudinal and radial strains are reduced, but circum-ferential strain and LV twist are preserved. LV ejection fractionand circumferential strain are the independent determinants of LV twist. The study was performed on a limited number of con-secutive patients. They were not perfectly matched for age,gender, and disease severity. The preliminary character of thereport was acknowledged in the manuscript.

It is common practice to subdivide patient with heart failure into those with systolic and diastolic heart failure, according to the ejection fraction. In systolic heart failure, the heart works by way of asubtle balance between a steep diastolic and a at, horizontal systolic pressurevolume relationship. The stroke volume is limitedby the inability to decrease systolic volume under workableblood pressures. The predominant abnormality of myocardial cellcontraction and the remodelling lead from the start to loss of torsion, i.e. loss of the wringing motion, as explained above. In diastolic heart failure, the heart works by way of a subtle balance

between a steep diastolic and an even steeper systolic pressure volume relationship ( Figure 1). Stroke volume is limited by theinability to increase diastolic volume and to decrease systolicvolume further. In early diastolic heart failure, torsion may beregarded as a compensatory mechanism to combined and balancedcontraction and relaxation abnormalities of the myocardial cell.

This compensation contributes to the preservation of the ejectionfraction. For example, pressure overload induced by aortic stenosisis associated with an increase of systolic LV wringing motion. Thismechanism, however, declines with increasing LV hypertrophy anddilatation.9 A similar compensation was observed in diabetic type Ipatients. 10 In the contribution under scrutiny, 1 torsion was as amean normal. This could suggest more advanced disease than in

the former two studies, heart failure with pseudonormalizationof torsion. It remains to be investigated how this pseudonormaliza- tion differs from normal physiological torsion.

In addition to quantitative aspects of twist, the rate and timing of twisting and untwisting should be further analysed. The untwistingof the heart predominantly occurs during isovolumetric relax-ation.11 Preservation or impairment of torsion during isovolu-metric relaxation can add to our insight on diastolic heart failure.In patients with hypertension and hypertrophy, diastolic untwistingis delayed and reduced, 12 but in diastolic heart failure untwisting ispreserved. 13 Such discrepancies should be claried.

We might speculate why circumferential strain parallels to someextent torsion in diastolic dysfunction, while longitudinal function isdepressed. Torsion is a contributor to circumferential strain inaddition to myocardial bre shortening. However, in the modelof Torrent-Guasp, torsion should be affected by longitudinal function as well, unless the downward systolic motion of the cardiacbase can be uncoupled from the torsion: in hypertrophy and diastolic dysfunction, combined torsion and longitudinal function haveevolved toward even increased torsion and loss of longitudinalfunction. This paradox should primarily be investigated with theanalysis of shear strains, but also in terms of the velocity, duration,and extent of longitudinal shortening, and in terms of re-orientation of myocardial bres in hypertrophy.

Further research should describe the contribution of torsion

and three-dimensional strains to the dysfunction in various stagesand aetiologies of cardiac failure. Gender differences should beactively searched for. While women tend to respond to overloadand injury by hypertrophy and brosis, men tend to respond moreby contractile dysfunction and dilatation. 14 The underlying mechan-isms of sex-related differences and hormonal effects on cardiacremodelling remain poorly investigated, but could be related todifferential constitutive nitric oxide synthase regulation and itseffects on the myocardium and coronary vasculature. 15 Thiscould manifest at early stages of the response to load or injuryas differential behaviour of torsion between men and women.

Finally, in the way that clinical researchers think and if possible in

their computations, they should not forget the importance of shear strains in addition to three-dimensional strains. 16 Only then will they be able to understand total deformation and function. Com-putation of longitudinal/circumferential shear is another promisingapproach to the assessment of torsion with speckle tracking, allow-ing in addition the investigation of regional differences in torsion. 17

Conict of interest: none declared.

References1. Wang J, Khoury DS, Yue Y, Torre-Amione G, Nagueh SF. Pre-

served left ventricular twist and circumferential deformation, butdepressed longitudinal andradial deformation in patients with

Figure 1 In systolic heart failure (left panel), the heart worksby way of a subtle balance between a steep diastolic and a at,horizontal systolic pressure volume relationship. Torsion isreduced. In diastolic heart failure (right panel), the heart worksby way of a subtle balance between a steep diastolic and aneven steeper systolic pressurevolume relationship. Torsion(arrow) is enhanced or normal.

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diastolic heart failure. Eur Heart J 2008;29 :12831289. First pub-lished on April 2, 2008. doi:10.1093/eurheartj/ehn141.

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4. Buckberg GD, Castella M, Gharib M, Saleh S. Active myocyteshortening during the isovolumetric relaxation phase of diastoleis responsible for ventricular suction; systolic ventricular lling.Eur J Cardiothorac Surg 2006;29 Suppl 1:S98106.

5. Sengupta PP, Krishnamoorthy VK, Korinek J, Narula J, Vannan MA,Lester SJ, Tajik JA, Seward JB, Khandheria BK, Belohlavek M. Leftventricular form and function revisited: applied translationalscience to cardiovascular ultrasound imaging. J Am Soc Echocardiogr 2007;20 :539551.

6. Buckberg GD, Coghlan HC, Hoffman JI, Torrent-Guasp F. Thestructure and function of the helical heart and its buttress wrap-ping. VII. Critical importance of septum for right ventricular function. Semin Thorac Cardiovasc Surg 2001;13 :402416.

7. Van de Veire N, De Sutter J, Bax JJ, Roelandt JRTC. Technologicaladvances: tissue Doppler imaging echocardiography. Heart 2008;doi:10.1136/hrt.2007.120758.

8. Helle-Valle T, Crosby J, Edvardsen T, Lyseggen E, Amundsen BH,Smith HJ, Rosen BD, Lima JA, Torp H, Ihlen H, Smiseth OA.New noninvasive method for assessment of left ventricular rotation: speckle tracking echocardiography. Circulation2005;112 :31493156.

9. Sandstede JJ, Johnson T, Harre K, Beer M, Hofmann S, Pabst T,Kenn W, Voelker W, Neubauer S, Hahn D. Cardiac systolicrotation and contraction before and after valve replacement for

aortic stenosis: a myocardial tagging study using MR imaging. AJR Am J Roentgenol2002;178 :953958.

10. Chung J, Abraszewski P, Yu X, Liu W, Krainik AJ, Ashford M,Caruthers SD, McGill JB, Wickline SA. Paradoxical increase in ventricular torsion and systolic torsion rate in type I diabetic patientsunder tight glycemic control. J Am Coll Cardiol2006;47 :384390.

11. Rademakers FE, Buchalter MB, Rogers WJ, Zerhouni EA, Weisfeldt ML, Weiss JL, Shapiro EP. Dissociation between left ventricular untwisting and lling. Accentuation by catecholamines. Cir-culation 1992;85 :15721581.

12. Takeuchi M, Borden WB, Nakai H, Nishikage T, Kokumai M,Nagakura T, Otani S, Lang RM. Reduced and delayed untwistingof the left ventricle in patients with hypertension and left ventricu-lar hypertrophy: a study using two-dimensional speckle trackingimaging. Eur Heart J 2007;28 :27562762.

13. Wang J, Khoury DS, Yue Y, Torre-Amione G, Nagueh SF. Left ventricular untwisting rate by speckle tracking echocardiography. Cir-culation 2007;116 :25802586.

14. Douglas PS, Katz SE, Weinberg EO, Chen MH, Bishop SP,Lorell BH. Hypertrophic remodeling: gender differences in theearly response to left ventricular pressure overload. J Am Coll

Cardiol 1998;32 :11181125.15. Loyer X, Oliviero P, Damy T, Robidel E, Marotte F, Heymes C,Samuel JL. Effects of sex differences on constitutive nitric oxidesynthase expression and activity in response to pressure overloadin rats. Am J Physiol Heart Circ Physiol2007;293 :H2650H2658.

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17. Ashikaga H, Criscione JC, Omens JH, Covell JW, Ingels NB Jr.Transmural left ventricular mechanics underlying torsional recoilduring relaxation. Am J Physiol Heart Circ Physiol2004;286 :H640H647.

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